Background: Adipokines are proteins which are secreted from the adipose tissue.These groups of proteins are involved in the control of metabolism. Chemerin is one of these adipokines with different proposed biological roles. Serum levels of chemerin have been associated with increased body mass index, insulin resistance, metabolic syndrome, diabetes and cardiovascular diseases. The aim of this study was to assess the association between serum chemerin concentrations and polycystic ovarian syndrome.Methods: This case-control study was performed in Taleghani Hospital in Tehran, Iran during 2011. On 45 patients with polycystic ovarian syndrome and 45 normal individuals as the control group. The participants were selected by easy given sampling method. Body mass index, fasting chemerin and serum insulin concentrations were measured by Enzyme-Linked Immunosorbent Assay (ELIZA) method. Fasting serum glucose was measured by the enzyme-calorimetric method and insulin resistance index (HOMA-IR) was measured by the calculation of relevant equation. Data was analyzed using independent t-test and Pearson’s correlation coefficient by SPSS version 18.Results: Serum chemerin, insulin, and glucose concentrations were significantly higher in patients with polycystic ovarian syndrome than the control group. There was no significant correlation between body mass index, serum levels of insulin, glucose, HOMA-IR, or chemerin in cases and controls.Conclusion: This study showed that serum chemerin levels increase in polycystic ovarian syndrome. The findings also suggest that changes in chemerin serum levels could be considered as a criterion for polycystic ovarian syndrome.

Background: Breast cancer is one of the major causes of cancer- related death and the most common solid malignancy in women worldwide. Chemerin as a new adipokine has an inflammatory activity that initiates inflammation via chemotaxis of immature DCs and macrophages. This study aimed to evaluate the level of chemerin in patients with breast cancer.Materials and Methods: In this cross-sectional study that was performed as a case- control study, we enrolled 45 patients with breast cancer in Vali-asr hospital from June to December 2015 (age range, 18-60 years) and 40 healthy volunteers as a control group (age range, 22-56 years). The patients with invasive breast were selected before mastectomy. The level of serum chemerin was measured by ELISA kit.Results: The results showed that the mean serum chemerin level in the breast cancer patients (1536 ±608 ng/L) was significantly lower than the normal individuals (1919±544 ng/L), (p=0.04). There is no correlation between the level of chemerin with body weight, stage of disease, duration of disease and the number of white and red blood cells.Conclusion: With due attention to the inflammatory role of chemerin, decreasing the serum chemerin level in patients with breast cancer may be related to the consumption of chemerin in the inflammatory responses or immunosuppression by tumor. The low level of chemrerin may be suitable for tumor growth and progression.

Objective(s): Chemerin is associated with insulin resistance, obesity, and metabolic syndrome. α-lipoic acid (α-LA) is a potent antioxidant involved in the reduction of diabetic symptoms. This study aimed to investigate the relationship between chemerin and P38 MAPK in the progression of diabetic nephropathy (DN) and examine the effects of α-LA on chemerin-treated human mesangial cells (HMCs). Materials and Methods: HMCs were transfected with a chemerin-overexpressing plasmid. HMCs were also treated with high-glucose, chemerin, α-LA, PDTC (pyrrolidine dithiocarbamate ammonium, NF-κ B p65 inhibitor), and/or SB203580 (P38 MAPK inhibitor). Cell proliferation was tested using the Cell Counting Kit-8 assay. Collagen type IV and laminin were tested by ELISA. Chemerin expression was detected by qRT-PCR. The chemerin receptor was detected by immunohistochemistry. Interleukin-6 (IL-6), tumor necrosis factor-a (TNF-α ), nuclear factor-κ Bp-p65 (NF-κ B p-p65), transforming growth factor-β (TGF-β ), and p-P38 mitogen-activated protein kinase (p-P38 MAPK) were evaluated by western blot. Results: High-glucose culture increased the expression of the chemerin receptor. α-LA inhibited HMC proliferation. Chemerin overexpression increased collagen type IV and laminin expression. P38 MAPK signaling was activated by chemerin, resulting in up-regulation of IL-6, TNF-α , NF-κ B p-p65, and TGF-β . SB203580, PDTC, and α-LA reversed the effects of chemerin, reducing IL-6, TNF-α , NF-κ B p-p65, and TGF-β expression. Conclusion: Chemerin might be involved in the occurrence and development of DN. α-LA might prevent the effects of chemerin on the progression of DN, possibly via the P38 MAPK pathway.